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Objective To enhance the clinical diagnosis efficiency and accuracy of diabetic retinopathy (DR) to facilitate its early finding and diagnosis.Methods Image segmentation method was used to process and analyze DR vessel.Clinical images by fundus fluorescein angiography (FFA) were used as the objects for the research on DR vessel segmentation and extraction.Results Image processing and analysis gained higher definition and accuracy in segmenting the normal retinal image and DR vessel when they were compared with the fundus image and FFA image.Conclusion The method proposed enhances the early diagnosis of DR by processing and analyzing the retinal vessel,and thus contributes to the increased living quality of the patient.
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Objective To study the liver protection of crocetin against paraquat (PQ) poisoning induced acute liver injury in rats. Methods Fifty-four male Wistar rats were randomly divided into control group, exposure group and treatment group, and the rats in each group were subdivided into the 0.5th, 2nd, and 6th day after exposure subgroups (n = 6). The model of acute liver failure induced by PQ poisoning was reproduced by intraperitoneal injection of 20 mg/kg of 20% PQ, and the rats in control group was injected with the same amount of normal saline. The rats in treatment group were given with intraperitoneal injection of 50 mg/kg crocetin after 0.5 day, once a day until they were sacrificed; the other two groups were injected with the same amount of normal saline. The rats in all groups were sacrificed at the corresponding time points, and blood was collected from inferior vena cava and hepatic tissue was harvested. Hematoxylin and eosin (HE) staining was used to observe the pathological changes in liver tissue on the 6th day under light microscope. Enzyme linked immunosorbent assay (ELISA) was used to detect the serum tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels. Reverse transcription-polymerase chain reaction (RT-PCR) was used to detect the mRNA expressions of inducible nitric oxide synthase (iNOS) and nuclear factor-κB (NF-κB). The activities of apoptosis related factors, including caspase-8, -9, -12, in hepatic tissue were determined on the 6th day with chromogenic substrate method. Results In the liver tissue of exposed group, extensive infiltration of the inflammatory cells and the diffuse fragments necrosis were visible, and the regeneration of the liver cells was not obvious, and severity of the injury in a time dependent way. In the treatment group, the structure of hepatic artery was visible, and the infiltration of necrosis, congestion and inflammatory cells were not obvious. On the 0.5th, 2nd, and 6th day, serum levels of IL-6 and TNF-α, the mRNA expressions of iNOS and NF-κB in liver tissue, and the caspase-8, -9, -12 activities on the 6th day in the exposure group and treatment group were significantly higher than those in the control group. And the parameters in treatment group were significantly lower than those of the exposure group [IL-6 (ng/L): 188.37±64.21 vs. 376.61±82.42 on the 0.5th day, 287.18±58.69 vs. 432.77±96.28 on the 2nd day, 234.24±10.17 vs. 375.41±37.59 on the 6th day; TNF-α (ng/L): 472.36±76.43 vs. 688.33±102.19 on the 0.5th day, 189.32±87.54 vs. 296.21±89.77 on the 2nd day, 99.28±16.13 vs. 168.41±66.78 on the 6th day; iNOS mRNA (gray value): 2.998±0.801 vs. 3.453±0.026 on the 0.5th day, 3.126±0.306 vs. 5.259±0.153 on the 2nd day, 0.841±0.135 vs. 1.225±0.057 on the 6th day; NF-κB mRNA (gray value): 1.569±0.818 vs. 2.361±0.063 on the 0.5th day, 2.345±0.489 vs. 4.668±0.368 on the 2nd day, 2.348±0.316 vs. 3.972±0.449 on the 6th day; caspase-8 (pmol/mg): 126.77±9.97 vs. 199.18±66.48 on the 6th day; caspase-9 (pmol/mg): 213.12±69.06 vs. 321.62±89.39 on the 6th day; caspase-12 (pmol/mg): 183.46±70.52 vs. 219.68±53.93 on the 6th day, all P < 0.05]. Conclusion Crocetin has protective effect on liver in rats with PQ poisoning, which role is related with reducing the blood level of inflammatory factors, inhibiting the hepatic caspase-8, -9, -12 activities and gene expressions of iNOS and NF-κB.
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As the main drug in colorectal cancer chemotherapy,oxaliplatin is gradually infiltrated into other malignancies therapy.But oxaliplatin-induced peripheral neuropathy limits its clinical application.The mechanisms of oxaliplatin neurotoxicity are not yet clear.Recent researches show that the acute neurotoxicity of oxaliplatin is mediated through changes in Na + transient conductances.And the function of the mitogen-activated protein kinases in chronic neuropathy has already been demonstrated in vitro.Furthermore,numerous indicators can be used to predict oxaliplatin-induced peripheral neuropathy,which bring the hope for improving the continuity of chemotherapy and realizing personalized medicine therapy.
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<p><b>OBJECTIVE</b>To investigate the effect of NG-nitro-L-arginine (L-NNA), a nitric oxide synthase (NOS) inhibitor, on the testis cell apoptosis in morphine-dependent rats induced by naloxone and the involved mechanisms.</p><p><b>METHODS</b>Forty-eight Wistar rats were randomly divided into a control group, withdrawal group and a therapeutic group. Morphine-dependent rats were given gradually increasing doses of morphine to produce morphine-dependent models, the abstinent syndrome precipitated by naloxone. The inhibiting effect of L-NNA on the abstinent syndrome, and the testis apoptosis, NOS positive cells, calmodulin (CaM) contents, superoxide dismutase (SOD) activity, and glutathione super oxidase (GSHPx) activity of the morphine-dependent rats induced by naloxone were observed and recorded by radioimmunoassay, atomic absorption spectrometry, in situ nick translation (ISNT) and NADPH-d histochemical technique.</p><p><b>RESULTS</b>Compared with the control rats, the function of the somesthetic motor nerves and autonomic nerves was excessive, the apoptosis and NOS positive cells in the testis were significantly increased (P < 0.05 or P < 0.01), the content of CaM and the activity of SOD and GSHPx were obviously decreased in the morphine-dependent rats induced by naloxone. But L-NNA could significantly inhibit the abstinent syndrome, decrease NOS positive cells and apoptosis, and increase CaM content and the activity of SOD and GSHPx in the testis.</p><p><b>CONCLUSION</b>Morphine dependence can induce testis cell apoptosis, an increase in testis NOS positive cells, a decrease in CaM content and the activity of SOD and GSHPx in the testis. L-NNA has the curative effect on the morphine abstinent syndrome, protects testis cells against apoptosis and improves their involved biochemical indexes.</p>
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Animals , Male , Rats , Apoptosis , Calmodulin , Disease Models, Animal , Morphine Dependence , Pathology , Nitric Oxide Synthase , Nitroarginine , Pharmacology , Random Allocation , Rats, Wistar , Spermatozoa , Testis , PathologyABSTRACT
Objective: To investigate the antagonistic effect of lithium on the neurotoxicity of lead acetate and the possible mechanisms. Method: Wistar rats were randomly divided into control group, Pb group and four Pb+ LiCl groups fed with feed containing 3, 30, 300, 3 000 mg/kg LiCl respectively. All Pb exposed groups were given distilled water containing 0.2% PbAc. The changes of nNOS protein and gene expression in rats hippocampus were studied by ABC immunohistochemistry and the semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) method. Rusults: Compared with the control group, the number of nNOS positive neurons in CA1 area and the nNOS mRNA content of hippocampus of LiCl (3, 30 mg/kg) groups were increased,while those of Pb-exposed rats were significantly decreased. Compared with Pb groups, the number of nNOS positive neurons and the nNOS mRNA content of Pb+LiCl (3,30,300 mg/kg) groups were increased. In dentate gyrus, the changes of the number of nNOS positive neurons coincided with the changes in CA1 area, but those in CA3 area showed little difference. Conclusion: Low dose of lithium could resist the lead neurotoxcity obviously.
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Objective: To study the effect of taurine to resist the impact of lead on learning and memory. Methods: ABC immunohistochemistry method was used to study the quantity change of nNOS positive neuron in hippocampus of the rats which were fed with distinct dosage of lead acetate in drinking water (0.02, 0.2 g/L) and distinct dosage of taurine (5,10 g/kg) in feed. Rusults: Taurine could increase nNOS positive neuron quantity obviously in hippocampus of rats induced by lead lesion. Conclusion: Taurine could resist impact of lead on learning and memory obviously.
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Objective:To observe the effects of zinc supplementation on the function of brain after sleep deprivation(SD).Methods:Rats SD model was made by the “Flower Pot" technique.Three days later,the rats received Y-labyrinth test to test the function of learning and memory.NADPH-d histochemistry and ABC immunohistochemistry were applied to exam the activity of NOS and the levels of protein expression of nNOS in hippocampus of rats.Results:Compared with the normal group,Learning times of rats in Y-labyrinth test of the SD group increased(89.3?25.3 /67.1?29.3,t=1.81,P0.05).Compared with the SD group,in TZC supplementation group,the levels of NOS in sub-area of hippocampus(CA_1:27.2?2.8;CA_3:15.3?1.6;DG:21.8?1.9,P0.05).Conclusions:TZC supplementation can improve learning and memory function of rats,and the mechanisms might be related to increased level of NOS and the protein expression of nNOS in hippocampus of animals.
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Objective To study the molecular mechanism about injurious effect of morphine dependence on the construction and function of hippocampal neurons. Method Mice were given (sc) increasing doses of morphine to form morphine-dependence model ,and the DNA and RNA changes stained with acridine orange (AO) fluorescence probe technique were investigated in hippocampal neurons of morphine-dependence group,naloxone-precipitated withdrawal group in morphine-dependence mice and control group. Results Compared with control group , the staining changes of DNA,RNA decreased obviously in hippocampal neurons of both morphine-dependence group and naloxone- precipitated withdrawal group in morphine-dependence mice,especially the later. Conclusion Both morphine-dependence and naloxone-precipitated withdrawal in morphine-dependence mice injured nucleic acid metabolism in hippocampal neurons ,especially the later.Those changes may be some reasons of decreased brain function ,especially in learning and memory deficits.
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Objective:To study the difference of c-fos expression of neurons in subareas of hippocampus of morphine dependent mice.Methods:Mice were given (sc) increasing doses of morphine to form morphine dependent models and withdrawal syndromes were precipitated by naloxone. The intensity of withdrawal syndromes was evaluted accoding to indices ,such as the number of jumping ,the weight loss,et al .The expression of Fos positive neurons in subareas of CA1, dentate gyrus and CA3 of hippocampus of morphine dependent group was observed by immunohistochemistry assay. Results:The number of Fos positive cells in subareas of CA1 and dentate gyrus of morphine dependent group was much higher than that of the normal control group(P
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Objective To study the antagonism of taurine-zinc coordination compound (TZC) to the adverse effect of mercury (Hg) on the neurons in the cerebral cortex. Methods 32 male Wistar rats aged 21days were randomly divided into 4 groups, one control group (fed on distilled water), three experimental groups fed on HgCl2 (0.06 g/L), HgCl2+0.23 g/L TZC and HgCl2+0.46 g/L TZC respectively, treated for one month. The NOS activity in the cerebral cortex neurons was determined by NADPH-d histochemistry. Results NADPH-d positive neurons increased in HgCl2 group (P
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Objective: To investigate the protective effect of zinc on learning and memory of lead-exposed rats and hippocampal SS and SS mRNA neurons. Met hods: Wistar rats were exposed to 6.15 mmol/L lead acetate solution or 6.15 mmol/L lead acetate and 3.10 mmol/L zinc sulfate solution for three months, and the learning and memory ability was studied with Y-maze test. The blood and hippocampal lead concentration were measured with atomic absorption spectrometry and the number of hippocampal SS and SS mRNA positive neur ons were observed with immunohistochemistry and in situ hybridization respectively. Results: Compared with the control and lead-zinc group, the learning and memory ability of lead-exposed rats was significantly decreased(P
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Objective: To explore the protection of taurine-zinic coordination compound(TZC) against the neurotoxicity of depleted uranium (DU). Method: Rats were exposed to DU by different dosages intratracheal instillation of DU particles. One group was supplemented with TZC. Learning times in Y-labyrinth experiment, number of somatostatin positive cortical neurons were compared. Results: Learning times in Y-labyrinth experiment were increased in DU groups, and DU 5mg+TZC group was less than that of DU 5 mg group (P
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Objective: To explore the effects of zinc (Zn) on neuronal nitric oxide synathase (nNOS) and somatostatin(SS) in cerebral cortex of rats after sleep deprivation (SD), and discuss the protective mechanism of Zn on learning and memory. Method: SD was induced in male Wistar rats by employing “flower pot” technique. The rats in SD+Zn groups were supplemented with Zn in feed (containing 200 mg Zn/kg)for 3 d before SD. The number of nNOS and SS positive neurons in cortex of rats after different time of SD and Zn supplementation were observed. Results: nNOS and SS positive neurons in cortex significantly decreased in SD1 d+Zn group than in SD1d group(P0.05). Conclusion: Zinc can improve the ability of learning and memory of rats after sleep deprivation by protecting nNOS and SS positive neurons in cerebral cortex.
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Objective: To explore the protective effects of zinc on learning and memory of mice suffering from acute repeated hypoxia. Method: 36 mice were divided into three groups randomly: normal control, saline+hypoxia (NS) group, zinc+hypoxia (Zinc) group. Model of acute repeated hypoxic mice was duplicated and the anoxia endurance was recorded. The step-through test and step-down test were used to evaluate the ability of learning and memory. Results: 1.Compared with saline+hypoxia group, the anoxia endurance was significantly increased in zinc+hypoxia group (P
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Objective:To study the effect of taurine on protection against lead toxicity in cultured cortex neurons. Methods:Put taurine and different concentrations of lead acetate in cultures of cortex neurons and observe the length of dendites and the growth activity of neurons. Results:At the concentration of 10-8 mol/l lead acetate the growth of cultured cortex neurons were decreased and even the cells died. Taurine at the concentration of 1.6?10-3 mol/L could protect against lead toxicity and promote neuron to grow. Conclusion:Taurine can protect from lead acetate toxicity in cultured cortex neurons.